Peter Frost's anthropology blog, with special reference to sexual selection and the evolution of skin, hair, and eye pigmentation

Thursday, February 19, 2009

Origins of male homosexuality - The germ theory

How does male homosexuality originate? More to the point, how does it perpetuate itself? According to Ed Miller, it results from a balanced polymorphism—a delicate balancing act where too much feminization of the male brain causes attraction to one’s own sex and too little causes indifference to one’s own children. This week, I will present an alternate explanation: Greg Cochran’s germ theory.

Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.

His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:

Critic: Is it not likely that human sexuality is in fact a bell curve, with "strict homosexual" on one end and "strict heterosexual" on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing).

Greg: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter? (source)

Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.

First we have to say what ‘common’ means, in this context. Common means common compared to the noise in the system. So 1% is very common: no disease caused by random mutations is anywhere near that common. 1 in 10,000 is surprisingly common, but there are one or two mutation-caused diseases that are in that ballpark, like Duchenne’s muscular dystrophy. Turns out that the gene involved in muscular dystrophy is maybe 20 times longer than the typical gene — there are more opportunities for typos. So 1 in 7000 boys have Duchenne’s muscular dystrophy — that’s as common as a ‘system noise’ disease gets. (Cochran 2004?)

Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.

The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.

Do we know of diseases in which there are very specific targets—in which certain cell types are damaged or destroyed while neighboring cells are left intact? Sure. In some cases, a pathogen targets a particular cell type and has little effect on anything else. Human parvovirus (also known as fifth disease) hits erythroid precursor cells (the cells that manufacture red cells) and temporarily inhibits red cell production. In type-I diabetes, it seems likely that Coxsackie virus infections (in people with a genetic predisposition, in which HLA type plays a major role) trigger an autoimmune disease that gradually (over a year or so) destroys the islet cells which produce insulin. Other cells are not much affected. (Cochran 2004?)

Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.

Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.

We can deduce a few things about the hypothetical agent causing homosexuality. First, it has a small, but not incredibly small, critical community size. That is the size of the clump of people required to keep the agent going. Some agents, ones in which infection results in permanent immunity, need a _large_ number of people, big enough that there are new infected people showing up by the time it circles the community. Measles for example requires almost half a million people in close proximity. An agent that causes a persistent infection can have a very small community size: I'd guess that Epstein-Barr has a CCS under 50.

Since some communities seem to have no homosexuality at all (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) we can be sure that this hypothetical agent has a critical community size larger than that of Epstein-Barr. More like chickenpox, which has a CCS of about 300 people. Not that I'm saying it _is_ chickenpox, mind you. (Cochran 2005)

Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).

As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.

This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).

Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:

Some time in the course of this winter, there came to our lodge one of the sons of the celebrated Ojibbeway chief, called Wesh-ko-bug, (the sweet)... This man was one of those who make themselves women, and are called women by the Indians. There are several of this sort among most, if not all the Indian tribes. They are commonly called A-go-kwa, a word which is expressive of their condition. This creature, called Ozaw-wen-dib, (the yellow head), was now near fifty years old, and had lived with many husbands. I do not know whether she had seen me, or only heard of me, but she soon let me know she had come a long distance to see me, and with the hope of living with me. She often offered herself to me, but not being discouraged with one refusal, she repeated her disgusting advances until I was almost driven from the lodge. (Desy, 1978)

Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:

Some of the disruptive factors implicated by empirical evidence are excess prenatal testosterone exposure (a major factor), prenatal stress, and exotic factors such as disruptive chemical agents. Infections proposed by Cochran may also disrupt development, but I do not know of any evidence that supports this assertion as of yet. (Cochran 2005)

15 comments:

Any idea in which trimester the pathogen would be most likely to have an impact on fetal brain development? I did some browsing over at the GSS and found that gay men were particularly likely to have been born in the month of June, which would put them in the first trimester of fetal development at the height of flu season.

Here we talk about it a bit, as one example of a common, unexplained fitness-reducing syndrome.

Peer-reviewed. Like that means a lot. I've had reviewers argue history from what they saw in a movie (Fiddler on the Roof as a guide to Jewish occupations in the Middle Ages). I've also had reviewers who don't believe that there _is_ such a thing as positive selection.

Over and over, people keep assuming that this hypothetical pathogen must act before birth. It might, but there is no reason that it would have to, and I'd say that the odds were against it: we're subject to a lot more infectious diseases after birth than before birth.

We know of examples in which post-birth infections ruin a particular subpopulation of neurons (Von Economo's encephalitis and dopaminergic neurons, also possibly narcolepsy) and that is all that would be required.

Origins of male homosexuality - The Vitamin D theorypeople with MS are more likely to be born in MayStudies of infectious disease have been unable to find a bacterium or virus that might cause MS, and diet has been ruled out as a factor in the disease. But a study of 40,000 MS patients from Canada, Great Britain, Denmark and Sweden have shown that people with MS are more likely to be born in May. Babies born at this time have gone through a period of rapid growth in the womb at the end of winter when the mother's vitamin D levels are at their lowest. On the other hand there are fewest births of people with MS in November when sunny summer holidays ensure that rapid growth in the womb is supported by plenty of vitamin D.[...]investigations by the Oxford team in collaboration with Canadian scientists have shown that MS is inherited preferentially through the female line as an “imprinted” gene. This explains why MS affects three or four women to every man.[...]It now seems likely that insufficient vitamin D is the crucial environmental factor that modifies the DRB1 gene into the imprinted form that causes MS and transmits it from one generation to the next. DRB1 is one of a family of HLA genes that code for structures on the surface of human white blood cells. And it is white blood cells that are involved in the “autoimmune” reaction that destroys the nervous system of MS sufferers.

The Oxford team believe that people with MS have white cells that are incorrectly programmed early in life. There are millions of different T-cells, a particular type of white cell produced in the thymus gland, each programmed to recognise and attack different types of invading bacteria and viruses. Ordinarily the T cells that might attack the body itself are deleted early in life in a stock-taking process. But this process can go wrong when certain genes that are normally masked by the imprinting process are mistakenly unmasked.

When a certain stage of pregnancy occurs during the winter a lack of available Vitamin D may "ruin a particular subpopulation of neurons" and produce homosexuality.

Evolution has stored vitamin D for getting through winter in the bodyfat, the breakdown and metabolism of adipose tissue in results in the stored vitamin D being released to supply the bodies requirements.

In the modern world there is no winter period of food scarcity and hence adipose tissue fails to release its stores of vitamin D.

A calorific deficit in the winter to induce the metabolism of fat stores is lacking for the first time.

There is no consensus yet on the timing of prenatal effects on human behavioral development. Below is a paragraph from C.C.C. Cohen-Bendahana,C. van de Beeka, & S.A. Berenbaum (2005). Prenatal sex hormone effects on child and adult sex-typed behavior: methods and findings. Neuroscience and Biobehavioral Reviews, 29, 353–384.

"Sensitive periods for organizational effects. It is widely accepted that organizational effects are maximal during circumscribed sensitive periods when the brain is developing, but the exact sensitive periods for human behavioral effects of sex hormones are not known. Weeks 8–24 of gestation have long been considered the key period [e.g., 21,22], given data showing a testosterone surge in male fetuses then [23]. Nevertheless, there is increasing recognition that there may be multiple sensitive periods, and that different brain regions (and thus different behaviors) may be affected by hormones at different times. There are only limited data on this issue in human beings [24,25], but ample data from other species, including primates, illustrate this point [8]. For example, as mentioned above, data from rhesus macaques show that androgen exposure early in gestation masculinizes different behaviors than exposure late in gestation [9].

There may be another sensitive period shortly after birth, associated with another peak in testosterone in male infants during postnatal months 1–5. Its significance for human behavior is not well studied, but some information can be gleaned from studies in infant male monkeys who exhibit the same early postnatal peak. Those studies show that neonatal testosterone is important for genital development [26,27], but there is not clear evidence for its role in behavioral development: neonatal testosterone has been found to affect mother-offspring interaction in one study of juveniles [28], but not in another study of infants [29], and not to affect sex-dimorphic play or sexual behavior [28–30]. Given continuing postnatal brain development, it would not be surprising to find that sex hormones continue to affect thebrain and behavior after birth."

Greg,

Your 2000 article does not do justice to the 'gay germ' theory (I've added a link to it in my post). It provides only a brief summary that leaves out many elements. When people ask me for a good description of this theory, I refer them to other documents available at The World of Greg Cochran.

Yes, peer review is the worst possible system -- except for the others. All of my published articles have benefited from peer review, often considerably so. Even when I disagree with a reviewer, I know there's a problem that has to be addressed somehow.

I agree that this pathogen could act after birth, but some male homosexuality must be due to pre-natal events. How else would you explain the correlation between male homosexuality and digit ratio (a marker of prenatal androgenization)?

Tod,

I've heard of the vitamin D theory of male homosexuality, but this is the first time I've seen the primary literature on this topic. I agree with the main point: until recently, we evolved in an environment where body fat was normally burned off in early spring, thus releasing significant amounts of vitamin D and other nutrients. I suspect a lot of vitamin D deficiency is due to the permanent maintenance of excess body fat.

The idea that genetic disease affect only 1 in 10,000 does not make sense considering that the birth defect rate is around 3% of births. The 2-3% homosexual rate is similar to the 3% birth defect rate, which suggests that homosexuality could be genetic in origin.

I agree that this pathogen could act after birth, but some male homosexuality must be due to pre-natal events. How else would you explain the correlation between male homosexuality and digit ratio (a marker of prenatal androgenization)?

It is possible that the stronger immune system of men with a high digit ratio is more likely to destroy their sexual 'search image' in over-reacting to an infection which leaves them with the 'default setting'. (Vitamin D is a potent inhibitor of the proinflammatory response)Shape regression on 2D : 4D ratio

Greg cites Henry Harpending as saying Bushmen aren't homosexual. I wonder about how honest Bushmen are about something like that. Especially as "daily life is pervaded with put-downs" in that society according to Cultural Diversity

Bushmen and Amerindians may have some reported cases of homosexuality, but am I wrong by thinking that it is not of the same magnitude that in the occidental societies? Everybody, scientist or not, seem to agree that true cases of genetic transgender are extremely rare, and that most of the homosexuality we see today is environmental and cultural in origin, even if this is denied.Cultural, which goes with political correctness, TV, education and sedentary lifestyle and environnmental, which goes with pesticides, antibiotics and hormones introduced in the food chain.

The authors noted one inconsistent result, with respect to non-twin brothers (not part of the data reported above). The rate of homosexuality was on 9.2% (13/142), significantly lower than the expected rate. (In the absence of environmental factors, the rate for non-twin brothers should be the same as for dizygotic twins.)

This is an silly argument, based on a total unwillingness to look at how culture shapes behavior. Romantic attraction is highly complex and culturally specific. There are numerous reasons having to do with the complexity of romantic attraction that characteristics conducive to homosexuality could be selected for. (It's actually pretty amazing that none of the solemn pseudo-scientists discussing these questions notice how attracted women tend to be to homosexual men). Depending on the cultural setting, those characteristics will be more or less expressed in actual homosexuality.

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"If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction" - not necessarily true. If the pathogen is (for example) chickenpox, then the gay man does not have lifelong infectivity. The neurological damage is merely a permanent byproduct of a temporary infection. Likewise, narcoleptics are not a reservoir of the pathogen that destroyed a small part of their hypothalamus.

Given that we are sure that same sex preference is not genetic (ie no gene) and no one is 100% sure what environ octal factor or factors cause same sex preference. This is as good a guess as any and every good theory starts with a good guess that can be tested scientifically.

Welcome to my blog! For the most part, this page will be an extension of my website, with comments relating to my research. But it will also branch out into more general discussions of human evolution.